Alcohol use disorders are estimated to account for 1.4% of the total world disease burden (Beaglehole, 2003). Alcohol dependence is pervasive in most societies; in the U.S. alone, approximately 18 million people (7%) of the population suffer from alcohol abuse or dependence. An estimated 100,000 deaths are associated with alcohol-related causes each year. The economic burden ascribed to alcohol use is estimated to be $185 billion in annual economic cost to the nation directly or indirectly (Li et al., 2004). The alcohol withdrawal syndrome (AWS) is a constellation of symptoms and signs that arises in alcoholdependent individuals, typically within 24-48 hours of consumption of their last drink. The incidence of alcohol withdrawal in the general population is thought to be low (5%) but is much higher in those undergoing treatment for alcohol abuse (86%) (Caetano et al., 1998). This group also presents significant clinical challenges and generates considerable cost related to hospitalization and extensive services (Rathlev et al., 2002). Acute alcohol ingestion has an inhibitory effect at N-methyl-D-aspartic acid (NMDA) receptors, reducing excitatory glutamatergic transmission (Mayo-Smith et al., 2004; Brathen et al., 2005), and has an agonistic effect at GABAA receptors. During prolonged exposure to alcohol, NMDA receptor number and function are upregulated and GABAA receptors are reduced in number and function, leading to tolerance (Tsai et al., 1995). The roles are reversed during abstinence, with enhanced NMDA receptor function leading to many of the symptoms and signs of the AWS. Converging evidence indicates that an acute disruption in glutamatergic neurotransmission may be associated with the symptoms of alcohol intoxication and withdrawal (Tsai and Coyle, 1998). Acamprosate, an abstinence promoting drug, acts as a functional glutamate antagonist by blocking the rise in glutamate that occurs during the AWS (Lingford-Hughes and Nutt, 2003).